GABAergic postsynaptic responses mediated by spontaneous and evoked neurotransmitter release are partially segregated, suggesting they may serve distinct roles in neuronal signaling.

The activity of a set of GABAergic neurons is causally linked with a locomotory pattern in moving animals, and the mechanisms underlying the neuromodulatory role of GABA are illuminated.

Accumulation of perineuronal nets around parvalbumin (PV)-positive inhibitory interneurons closes visual cortical plasticity by selectively down-regulating thalamic synapses onto PV cells in a sensory-dependent manner.

Two genetically distinct Stxbp1 haploinsufficiency mouse models exhibit seizures and impairments in cognitive, psychiatric, and motor functions, representing robust preclinical models of STXBP1 encephalopathy with both construct and face validity.

Loss of Kirrel3 selectively reduces DG-GABA mossy fiber filopodia and causes CA3 neuron hyper-activity during brain development.

Placing the PACAP/PAC1 signaling within glutamate/GABA cell type and subregional contexts in mouse brain reveals its conspicuous role for sensorimotor circuit interaction through modulating neuronal plasticity.

The transcriptional cofactor HPK-1 (homeodomain-interacting protein kinase) functions as a key regulator of multiple proteostatic stress responses, each originating from discrete neuronal subtypes within the Caenorhabditis elegans nervous system to preserve neuronal health and maintain organismal proteostasis during normal aging.

Investigation of synapse development using a single neuron system illuminates how individual neurons specify connectivity with their postsynaptic partners and the central role of the synaptic organizer neurexin in this process.

Targeted genetic silencing and reporter labeling reveal that Purkinje cell activity organizes cerebellar basket cells into zonal modules based on the sizes of their projections.

Chronic perturbations of spiking activity trigger compensatory changes in GABAergic synaptic strength, but not compensatory changes in AMPAergic synaptic strength.